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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression data in over expressed Human Fetal Lung Fibroblasts with IPF downregulated miRNAs

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition.miRNA let-7d and mir30b were found to be signifcantly down regulated in IPF. Compared to control we over expressed these miRNAs in Human Fetal Lung Fibroblast cell line Fetal lung tissues were collected through the University of Pittsburgh Tissue Bank through approved IRB protocol 0506140. The samples were de-identified using an honest broker system and immediately transferred to the IRB exempt protocol PRO09040459 (PI: D. Carlisle). Total RNA was labeled with Cy3 and hybridized on Agilent 8X44K gene expression array (Agilent Technologies, Santa Clara, CA). After 17 hours hybridization, arrays were washed and scanned according to the manufacturer’s protocol.

ORGANISM(S): Homo sapiens

SUBMITTER: Luai Huleihel

PROVIDER: E-GEOD-38530 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Gene expression data in over expressed Human Fetal Lung Fibroblasts with IPF downregulated miRNAs

Project description:Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition.miRNA let-7d and mir30b were found to be signifcantly down regulated in IPF. Compared to control we over expressed these miRNAs in Human Fetal Lung Fibroblast cell line

2013-06-06 | GSE38530 | GEO

miRNA expression data in idiopathic pulmonary fibrosis

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2010-04-23 | E-GEOD-13316 | biostudies-arrayexpress

MicroRNA expression data in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition. Using miRNA expression microarrays we identified 96 differentially expressed miRNA in IPF lungs which included let-7d, miR-30 family, miR-29 family and miR-154 family. Lung tissue samples for microarray analysis were obtained through the University of Pittsburgh Health Sciences Tissue Bank. 13 samples were obtained from surgical remnants of biopsies or lungs explanted from patients with IPF who underwent pulmonary transplant, and 12 control normal lung tissues obtained from the disease free margins with normal histology of lung cancer resection specimens. The morphologic diagnosis of IPF was based on typical microscopic findings consistent with usual interstitial pneumonia. Total RNA was labeled with Cy3 and hybridized on Agilent 8X15K microRNA array (Agilent Technologies, Santa Clara, CA). After 20 hours hybridization, arrays were washed and scanned according to the manufacturer’s protocol.

2013-01-04 | E-GEOD-27430 | biostudies-arrayexpress

MicroRNA expression data in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition. Using miRNA expression microarrays we identified 96 differentially expressed miRNA in IPF lungs which included let-7d, miR-30 family, miR-29 family and miR-154 family.

2013-01-04 | GSE27430 | GEO

miRNA expression data in idiopathic pulmonary fibrosis

2010-04-23 | GSE13316 | GEO

Forkhead Box F1 (FOXF1) represses fibroblast functions relevant to fibrogenesis

Project description:Aberrant expression of master phenotype regulators by lung fibroblasts may play a central role in idiopathic pulmonary fibrosis (IPF). Interrogating IPF fibroblast transcriptome datasets, we identified Forkhead Box F1 (FOXF1), a DNA-binding protein required for lung development, as a candidate actor in IPF. Thus, we determined FOXF1 expression levels in fibroblasts cultured from normal or IPF lungs in vitro, and explored FOXF1 functions in these cells using transient and stable loss-of-function and gain-of-function models. FOXF1 mRNA and protein were expressed at higher levels in IPF compared with controls. In normal lung fibroblasts, FOXF1 repressed key fibroblast functions such as proliferation, survival, and expression of collagen-1 (COL1) and actin related protein 2/3 complex, subunit 2 (ARPC2). ARPC2 knockdown mimicked FOXF1 overexpression with regard to proliferation and COL1 expression. FOXF1 expression was induced by the antifibrotic mediator prostaglandin E2 (PGE2). Ex vivo, FOXF1 knockdown conferred CCL-210 lung fibroblasts the ability to implant and survive in uninjured mouse lungs. In IPF lung fibroblasts, FOXF1 regulated COL1 but not ARPC2 expression. In conclusion, FOXF1 functions and regulation were consistent with an antifibrotic role in lung fibroblasts. Higher FOXF1 levels in IPF fibroblasts may thus participate in a compensatory response to fibrogenesis. Lung fibroblasts derived from 4 different IPF patients (P313, P355, P375 and P426) were transiently transfected with pcfoxf1 or control pcDNA3.1-constructs. Total RNAs were extracted 24 h after transfection and hybridized on microarrays. One color experiment with 2 experimental conditions: pcfoxf1 and pcDNA3.1

2014-10-01 | E-GEOD-52612 | biostudies-arrayexpress

Compulsory expression of miR-210 in normal endometrial stromal cells

Project description:Compulsory expression of miR-210 in normal endometrial stromal cells directed the induction of cell proliferation and vascular endothelial growth factor production, and the inhibition of apoptosis in through signal transducer and activator of transcription 3 (STAT3) activation. Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-210, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-210 were identified by Compulsory expression of miR-210 in normal eutopic endometrial stromal cells, a global mRNA microarray technique, and Ingenuity pathways analysis. NESCs were transfected with precursor hsa-miR-210 (Pre-miRTM miRNA precursor- hsa-miR-210, Ambion, Austin, TX, USA) or negative control precursor miRNA (Pre-miRTM miRNA precursor-negative control #1 Ambion) at a final concentration of 10 nM, using LipofectamineTM RNAiMAX (Invitrogen, Carlsbad, CA, USA). Forty-eight hours after transfection, total RNA from cultured NESCs transfected with precursor hsa-miR-210 (n=4) and NESCs (n=4) transfected with negative control precursor miRNA was extracted with an RNeasy Mini kit (Qiagen, Valencia, CA, USA). Then, the samples were subjected to a gene expression microarray analysis with a commercially available human mRNA microarray (G4845A, Human Gene Expression 4x44K v2, Agilent Technologies, Santa Clara, CA, USA).

2015-04-06 | E-GEOD-56854 | biostudies-arrayexpress

cDNA microarray analysis of miR-1 transfected HeLa and NPC-TW01 cells

Project description:To investigate the mechanisms of miR-1 inducing apoptosis, we performed cDNA expression microarray analysis to identify the candidate miR-1 regulating genes that are involved in apoptosis. NPC-TW01 cells were transfected with miR-1 or miR-negative control for 40 hours, their total RNA were isolated from the cells and hybridized to an Agilent human whole genome oligo 4 x 44 K microarray. HeLa cells were transfected with miR-1 or miR-negative control for 40 hours, their total RNA were isolated from the cells and hybridized to an Agilent human whole genome oligo 4 x 44 K microarray.

2011-04-13 | E-GEOD-28522 | biostudies-arrayexpress

Increased Cell Surface Fas Expression is Necessary to Sensitize Lung Fibroblasts to Fas Ligation-Induced Apoptosis: Implications for Fibroblast Accumulation in Idiopathic Pulmonary Fibrosis.

Project description:Idiopathic pulmonary fibrosis (IPF) is associated with the accumulation of collagen-secreting fibroblasts and myofibroblasts in the lung parenchyma. Many mechanisms contribute to their accumulation, including resistance to apoptosis. In previous work, we showed that exposure to the pro-inflammatory cytokines, TNF-α and IFN-γ reverses fibroblast resistance to apoptosis. The goal of this study was to investigate the underlying mechanism. Based on an initial interrogation of the transcriptomes of unstimulated and TNF-α and IFN-γ-stimulated primary lung fibroblasts and the lung fibroblast cell line, MRC5, we show here that among Fas-signaling pathway molecules, Fas expression was increased ~6-fold in an NF-κB and p38mapk-dependent fashion. Prevention of the increase in Fas expression using Fas siRNAs blocked the ability of TNF-α and IFN-γ to sensitize fibroblasts to Fas ligation induced-apoptosis; while enforced adenovirus-mediated Fas overexpression was sufficient to overcome basal resistance to Fas-induced apoptosis. Examination of lung tissues from IPF patients revealed low to absent staining of Fas in fibroblastic cells of fibroblast foci. Collectively, these findings suggest that increased expression of Fas is necessary and sufficient to overcome the resistance of lung fibroblasts to Fas-induced apoptosis. They also suggest that approaches aimed at increasing Fas expression by lung fibroblasts and myofibroblasts may be therapeutically relevant. To investigate the mechanism by which TNF-α and IFN-γ reprogram fibroblasts from resistance to sensitivity to Fas-ligation-induce apoptosis, we exposed human primary lung fibroblasts from an IPF patient (FS087) and non-disease control subject (N78) and the human fetal lung fibroblast cell lung (MRC-5) to TNF-α (10 ng/ml) and IFN-γ (50 U/ml) for 36 hr and analyzed changes in their transcriptomes using Affymetrix microarrays.

2011-01-13 | E-GEOD-26594 | biostudies-arrayexpress

microRNA expression profiles in Idiopathic Pulmonary Fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF) is a lethal fibrotic lung disease characterized by enhanced fibroblast proliferation, collagen synthesis, extracellular matrix deposition. We obtained 28 IPF patient lung tissue samples from the Lung Tissue Research Consortium (LTRC). Here we determined the miRNA expression profiles in these IPF lung samples.

2019-04-02 | GSE129126 | GEO

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